Many thanks to Suzanne O’Sullivan for her time in putting this podcast together. Her excellent books “It’s all in your head” and “Brainstorm” are well worth a read.
It is certainly one of the PHEMcast recordings which is going to change my own practice the most.
We can all find these patient’s challenging to look after – we often fail to communicate effectively and meaningfully. This is understandable as so much of our training and experience is based around the treatment of the physical condition.
The key things I took away from this interview were:
A vast majority of patients with psychosomatic symptoms have no control over their symptoms: even when they are made aware that there is no physical / pathological cause
By attributing psychosomatic symptoms to physical causes we are doing our patients a huge disservice
The sooner a psychosomatic cause for symptoms is identified and discussed with the patient the more likely they are to make a recovery
The misdiagnosis rate of a psychosomatic cause is low
There are several features of dissociative seizures that can help us distinguish them from true epileptic seizures
‘Malingering’ (pretending to be unwell for gain) is extremely rare
There are a huge number of terms to describe psychosomatic illness – some of which are not useful. A common nomenclature here will help communication between both health care professionals and our patients.
Psychosomatic: a physical illness or other condition) caused or aggravated by a mental factor such as internal conflict or stress.
Non-epileptic seizures = dissociative seizures.
The terms ‘functional’ and ‘supratentorial’ are best avoided!
These are a guide only, each patient will need a bespoke approach depending on their pre-existing condition, degree of cardiovascular compromise, conscious level and drugs already administered. Clearly you also need to remain within your scope of practice and the guidelines for your organisation.
For analgesia (IV/IO): 0.1 – 0.5mg/kg
For analgesia (IN): 3mg/kg
For sedation (IV/IO): 1mg/kg
For sedation (IM): 4-5mg/kg
For anaesthesia (IV): 1-2mg/kg
Click here for an example of how ketamine can affect patients.
Know the concentration you carry!
Click here for an example of what can occur if the incorrect concentration of ketamine is administered.
The PICHFORK (Pain in Children Fentanyl or Ketamine) Trial: A Randomized Controlled Trial Comparing Intranasal Ketamine and Fentanyl for the Relief of Moderate to Severe Pain in Children With Limb Injuries. YMEM. American College of Emergency Physicians; 2015 Mar 1;65(3):248–254.e1.
McQueen C, Crombie N, Cormack S, Wheaton S. Prehospital use of ketamine for analgesia and procedural sedation by critical care paramedics in the UK: a note of caution? Emergency Medicine Journal. 2014 Dec;31(12):1029.
Jennings PA, Cameron P, Bernard S, Walker T, Jolley D, Fitzgerald M, et al. Long-term pain prevalence and health-related quality of life outcomes for patients enrolled in a ketamine versus morphine for prehospital traumatic pain randomised controlled trial. Emergency Medicine Journal. 2014 Oct;31(10):840–3.
Andolfatto G, Abu-Laban RB, Zed PJ, Staniforth SM, Stackhouse S, Moadebi S, et al. Ketamine-propofol combination (ketofol) versus propofol alone for emergency department procedural sedation and analgesia: a randomized double-blind trial. Ann Emerg Med. 2012 Jun 1;59(6):504–12.e1–2.
Jennings PA, Cameron P, Bernard S, Walker T, Jolley D, Fitzgerald M, et al. Morphine and Ketamine Is Superior to Morphine Alone for Out-of-Hospital Trauma Analgesia: A Randomized Controlled Trial. Ann Emerg Med. 2012 Jan 11.
Bredmose PP, Lockey DJ, Grier G, Watts B, Davies G. Pre-hospital use of ketamine for analgesia and procedural sedation. Emerg Med J. 2009;26(1):62–4.
Howes MC. Ketamine for paediatric sedation/analgesia in the emergency department. Emerg Med J. 2004 May 1;21(3):275–80.
Porter K. Ketamine in prehospital care. Emerg Med J. 2004 May 1;21(3):351–4.
Gunning M, Perkins Z, Quinn T. Trench entrapment: is ketamine safe to use for sedation in head injury? Emerg Med J. 2007 Nov 1;24(11):794–5.
McGlone RG, Howes MC, Joshi M. The Lancaster experience of 2.0 to 2.5 mg/kg intramuscular ketamine for paediatric sedation: 501 cases and analysis. Emerg Med J. 2004 May 1;21(3):290–5.
Roback MG, Wathen JE, MacKenzie T, Bajaj L. A randomized, controlled trial of i.v. versus i.m. ketamine for sedation of pediatric patients receiving emergency department orthopedic procedures. Ann Emerg Med. 2006 Nov 1;48(5):605–12.
Newton A, Fitton L. Intravenous ketamine for adult procedural sedation in the emergency department: a prospective cohort study. Emerg Med J. 2008 Aug 1;25(8):498–501.
If you would like to read more, there is a blog post Martin and I wrote here on the subject of dizziness, including some videos demonstrating elements of the HINTS exam, and another one from the St Emlyns team.
The Munroe-Kellie Doctrine is illustrated by the following pictures:
Or, alternatively, by Elfyn’s pint of Guinness analogy!
Allows giraffes to drink from pools without a rush of blood to the head and eat leaves from trees without fainting.
This graph shows what happens to cerebral arterioles in uninjured brains, taken from Researchgate.net (Pires et al., 2013.)
Without autoregulation, in an injured brain, the arterioles will not change diameter in response to variations in blood pressure, and cerebral blood flow will have a linear relationship with blood pressure.
Cerebral perfusion pressure
Cerebral perfusion pressure = Mean arterial pressure – intracerebral pressure
The diameter of the arterioles, and therefore Cerebral perfusion pressure, is also affected by extremes of oxygen and carbon dioxide. If you would like to read more about this, have a look at this Life in The Fast Lane post.
The Brain Injury Foundation guidelines which Fliss mentions can be accessed here.
Doubts over head injury studies. Roberts I, Smith R, Evans S. BMJ. 2007 Feb 24; 334(7590): 392–394. (This is the paper Elfyn mentions regarding the now redacted original publications on the use of mannitol)
Another invitation to the Trauma Care Conference this year inspired us to combine two of the excellent speakers into this podcast considering major incidents. Thanks to both our speakers for sharing their talks from the conference.
Trauma Care offer more than the annual conference; there are monthly webinars and regional meetings too, click here for more information.
The Joint Emergency Services Interoperability Programme (JESIP) website and National Ambulance Resilience Unit (NARU) website have lots of resources to support your response to a major incident.
The papers which Chris mentions regarding IED injury patterns and management in children are both from the Journal of the Royal Army Medical Corps:
Cardiac arrest is the end point, it is the symptom, not the diagnosis. The pathophysiological process varies, and this is particularly relevant in trauma vs medical. In medical cardiac arrest, the pathological processes tend to affect the heart’s ability to pump: eg primary cardiac event, chemical/electrolyte abnormality, but full circulation. In trauma the process is generally not primarily due to pump failure, but due to hypovolaemia or obstruction. It might be better to consider traumatic cardiac arrest as a completely different disease eg LOST: Low Output State due to Trauma
The 2015 European Resuscitation Council and UK Resuscitation Council Algorithms for Traumatic Cardiac Arrest:
To read the whole ERC guideline on special circumstances cardiac arrest including trauma, click here.
Ultrasound during TCA: Cureton et al. The heart of the matter: utility of ultrasound of cardiac activity during traumatic arrest. J Trauma. 2012; 73: 102-10.
The outcomes from different resuscitative interventions in a haemorrhagic shock model in porcine model:
From: Watts et al. Closed chest compressions reduce survival in a model of haemorrhagic-induced traumatic cardiac arrest . EMJ 2017; 34: 860-900. (A866)
Impact brain apnoea: Wilson et al. Impact brain apnoea – A forgotten cause of cardiovascular collapse in trauma. Resuscitation. 2016; 105: 52-58.
Barnard et al. Epidemiology and aetiology of TCA in England… Resuscitation; 110 (2017): 90-94.
Russell RJ et al. The role of trauma scoring in developing trauma clinical governance in the Defence Medical Services. Phil Trans R Soc. 2011; 366. Doi: 1098/rstb.2010.0232
Wise et al. Emergency thoracotomy ‘how to do it’. EMJ; 2005: 22-24.
Morrison et al. Resuscitative thoracotomy following wartime injury.
Jeffcoach DR et al. Use of CPR in hemorrhagic shock, a dog model.
Lockey et al. Traumatic cardiac arrest: who are the survivors? Annals of Emergency Medicine; 2006.
Grasner et al. Cardiopulmonary resuscitation in traumatic cardiac arrest – there are survivors. Critical Care; 2011.
Zwingmann et al. Survival and neurological outcome after OOH TCA in pediatric & adult populations: a systematic review. Critical Care; 2012.
Slessor et al. To Be Blunt: are we wasting our time? Emergency Deaprtment Thoracotomy following blunt trauma: a systematic review & meta-analysis. Anneals of EM; 2015: 297-307.
Leis CC et sl. TCA: should advanced life support be initiated? J Trauma. 2013; 74: 634-8.
Jacobs et al. Effect of adrenaline on survival in out of hospital cardiac arrest: randomised double-blind placebo controlled trial. Resuscitation. 2011; 82: 1138-43.
Smith et al. Traumatic Cardiac Arrest. Journal of Royal Society of Medicine. 2015; 108: 11-16.
Sperry et al. Early use of vasopressors after injury: caution before constriction. J Trauma. 2008; 64: 9-14/
We recommend reading Atul Gawande’s book ‘The Checklist Manifesto’. It’s a well written, fascinating story about the introduction of the WHO Safer Surgery checklist and the impact it had. This link will take you straight to Amazon if you want to buy a copy (other internet retailers exist!!)
To understand the how human factors failed in the death of Martin’s wife, Elaine, please watch this video:
The fabulous Life in the Fast Lane have also produced a blog on the case.
There are lots of resources available on the Clinical Human Factors Group website.
Where can you undertake decompression of a pneumothorax?
Be particularly careful when using the 2nd intercostal space mid-clavicular line that you are sufficiently lateral. For example, here are the locations identified as ‘2nd ICS mid clavicular line’ amongst 25 EM physicians in a 2005 EMJ paper.
The Three Kings: George Clooney’s recommended approach to decompression of a tension pneumothorax. Note – again please do not use this location!
Devices used for decompression:
14G venous cannula
Dressings available for covering an open pneumothorax +/- thoracostomy in a spontaneously breathing patient:
Ball, C. G., Wyrzykowski, A. D., Kirkpatrick, A. W., Dente, C. J., Nicholas, J. M., Salomone, J. P., et al. (2010). Thoracic needle decompression for tension pneumothorax: clinical correlation with catheter length. Canadian Journal of Surgery Journal Canadien De Chirurgie, 53(3), 184–188.
Barton, E. D., Epperson, M., Hoyt, D. B., Fortlage, D., & Rosen, P. (1995). Prehospital needle aspiration and tube thoracostomy in trauma victims: a six-year experience with aeromedical crews. The Journal of Emergency Medicine, 13(2), 155–163.
Beckett, A., Savage, E., Pannell, D., Acharya, S., Kirkpatrick, A., & Tien, H. C. (2011). Needle Decompression for Tension Pneumothorax in Tactical Combat Casualty Care: Do Catheters Placed in the Midaxillary Line Kink More Often Than Those in the Midclavicular Line? The Journal of Trauma, 71, S408–S412. http://doi.org/10.1097/TA.0b013e318232e558
Cullinane, D., Morris, J., Bass, J., & Rutherford, E. (2001). Needle thoracostomy may not be indicated in the trauma patient. Injury, 32, 749–752.
Ferrie, E. P., Collum, N., & McGovern, S. (2005). The right place in the right space? Awareness of site for needle thoracocentesis. Emergency Medicine Journal, 22(11), 788–789. http://doi.org/10.1136/emj.2004.015107
Fitzgerald, M., Mackenzie, C. F., Marasco, S., Hoyle, R., & Kossmann, T. (2008). Pleural decompression and drainage during trauma reception and resuscitation. Injury, 39(1), 9–20. http://doi.org/10.1016/j.injury.2007.07.021
Givens, M. L., Ayotte, K., & Manifold, C. (2004). Needle thoracostomy: implications of computed tomography chest wall thickness. Academic Emergency Medicine : Official Journal of the Society for Academic Emergency Medicine, 11(2), 211–213. http://doi.org/10.1197/j.aem.2003.09.015
Harcke, H. T., Mabry, R. L., & Mazuchowski, E. L. (2013). Needle thoracentesis decompression: observations from postmortem computed tomography and autopsy. Journal of Special Operations Medicine : a Peer Reviewed Journal for SOF Medical Professionals, 13(4), 53–58.
Inaba, K., Branco, B. C., Eckstein, M., Shatz, D. V., Martin, M. J., Green, D. J., et al. (2011). Optimal positioning for emergent needle thoracostomy: a cadaver-based study. The Journal of Trauma, 71(5), 1099–103– discussion 1103. http://doi.org/10.1097/TA.0b013e31822d9618
Inaba, K., Ives, C., McClure, K., Branco, B. C., Eckstein, M., Shatz, D., et al. (2012). Radiologic evaluation of alternative sites for needle decompression of tension pneumothorax. Archives of Surgery (Chicago, Ill : 1960), 147(9), 813–818. http://doi.org/10.1001/archsurg.2012.751
Jadder, U., & McAuley, D. (2005). Transthoracic ultrasonography to diagnose pneumothorax in trauma. BestBETS.org, 1–3.
Jones, R., & Hollingsworth, J. (2002). Tension pneumothoraces not responding to needle thoracocentesis. Emergency Medicine Journal, 19, 176–177.
MD, A. R. M., MD, M. E. R., MD, C. S. C., & MD, J. L. M. (2015). Ultrasound determination of chest wall thickness: implications for needle thoracostomy. The American Journal of Emergency Medicine, 1–5. http://doi.org/10.1016/j.ajem.2010.06.030
MD, E. J. C., MD, C. H. C., BS, R. M., PHD, C. L. A., RDMS, C. A. K. M. M., RDMS, S. S. M., & RDMS, J. C. F. M. (2013). Ultrasound in Emergency Medicine. The Journal of Emergency Medicine, 44(1), 142–149. http://doi.org/10.1016/j.jemermed.2012.02.032
Netto, F. A. C. S., Shulman, H., Rizoli, S. B., Tremblay, L. N., Brenneman, F., & Tien, H. (2008). Are needle decompressions for tension pneumothoraces being performed appropriately for appropriate indications? The American Journal of Emergency Medicine, 26(5), 597–602. http://doi.org/10.1016/j.ajem.2007.08.016
Rathinam, S., Grobler, S., Bleetman, A., Kink, T., & Steyn, R. (2014). Evolved design makes ThoraQuik safe and user friendly in the management of pneumothorax and pleural effusion. Emergency Medicine Journal, 31(1), 59–64. http://doi.org/10.1136/emermed-2012-201821
Rathinam, S., Quinn, D. W., Bleetman, A., Wall, P., & Steyn, R. S. (2011). Evaluation of ThoraQuik: a new device for the treatment of pneumothorax and pleural effusion. Emergency Medicine Journal, 28(9), 750–753. http://doi.org/10.1136/emj.2009.082297
Sanchez, L. D., Straszewski, S., Saghir, A., Khan, A., Horn, E., Fischer, C., et al. (2011). Anterior versus lateral needle decompression of tension pneumothorax: comparison by computed tomography chest wall measurement. Academic Emergency Medicine : Official Journal of the Society for Academic Emergency Medicine, 18(10), 1022–1026. http://doi.org/10.1111/j.1553-2712.2011.01159.x
Yamagiwa, T., Morita, S., Yamamoto, R., Seki, T., Sugimoto, K., & Inokuchi, S. (2012). Determination of the appropriate catheter length for needle thoracostomy by using computed tomography scans of trauma patients in Japan. Injury, 43(1), 42–45. http://doi.org/10.1016/j.injury.2010.11.022
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Firstly, go and read Simon and Tim Harris’ great 2005 paper on the subject which we reference repeatedly in the podcast. It is available free open access here.
A pneumothorax exists when air accumulates in the potential space between the visceral and parietal pleura:
A tension pneumothorax exists when the air in the pleural cavity is under high pressure resulting in compression of the surrounding structures.
Simon mentions Rutherford’s diagram in the podcast. This is taken from a 1968 paper examining the progressive pathophysiology of a tension pneumothorax. The graph shows the changes in intrapleural pressure (on the ipsilateral and contralateral sides) in spontaneously breathing goats who had air injected into one side of their chest. We can’t find the full article free/open access anywhere I’m afraid. But this is the reference: THE PATHOPHYSIOLOGY OF PROGRESSIVE, TENSION PNEUMOTHORAX. Rutherford RB, Hurt HH, Brickman RD, Tubb JM. Journal of Trauma and Acute Care Surgery, March 1968,8(2):212-227
The imaging findings of tension pneumothorax might look like this:
% or partial pressure of carbon dioxide measured somewhere near the mouth at the end of a normal exhalation (hence end tidal, end of tidal volume breath)
To get a measurement the following systems need to be functioning:
Metabolically active tissue to produce CO2
Circulation & cardiac output to carry that CO2 to the lungs in blood
Transfer of CO2 between the blood and the air in the lung
Gas in and out of the lung to excrete the CO2
Brilliant monitor in anaesthesia in that in elective cases, we start off with healthy patients are looking for deviations from the norm- and a normal ETCO2 trace tells you that all those components are functioning.
It is still extremely useful in prehospital care, but we just have to remember that an abnormal trace or value may be caused by problems with one or more of those systems i.e circulation, gas exchange, ventilation (rarely tissue metabolism)
Much better than pulse oximetry, because of the difference in lag time between clinical change occurring and being able to see it on the monitor- less than 3 seconds for sidestream capnography, compared to up to 90s for pulse oximetry
How does ETCO2 relate to arterial CO2?
What we’re REALLY interested in is arterial CO2 as this is the clinically significant value in a number of clinical scenarios; for example in the brain-injured patient, we want to keep arterial CO2 values normal as we know that this determines the state of cerebral vasoconstriction or dilation, and thus affects ICP. In non-brain injured patients, high arterial CO2 can lead to a respiratory acidosis, and low pH values are harmful to most body tissues, in particular the clotting cascade (because of its reliance on enzymes, which function best in a narrow range of pH), and cardiac contractility.
In healthy people, ETCO2 is usually 0.5-1kPA LOWER than the arterial value. Why is this? CO2 is only found in parts of the lung which participate in gas exchange, i.e are perfused with blood. So the trachea and first few generations of bronchi do not participate in gas exchange and are known as the dead space. They ARE however filling with gas during breaths, and as such gas from this dead space DILUTES the gas containing CO2 that has come predominantly from the alveoli.
What we are assuming when we ask ETCO2 to substitute for arterial CO2 is that there is normal matching of ventilation to perfusion occurring in the lungs, so that all the mixed venous CO2 returning to the lungs from respiring tissue can equilibrate with alveolar gas and be eliminated via ventilation
What causes a discrepancy between arterial and ETCO2?
Loose connections, not having nasal prongs up nose, dilution with high oxygen flows (partic when using nasal prongs)
Failure of venous CO2 to cross to ventilated alveoli
Alveolar dead space- alveoli are ventilated but not perfused
Classically low cardiac output states, PE, etc
Failure of alveolar gas to be transported out of the lungs because alveoli are perfused but not ventilated (shunt):
pneumonia and pulmonary edema, pulm haemorrhage (alveoli filled with fluid)
tissue trauma: alveolar wall swelling
atelectasis: collapse of alveoli from failure to expand, or absorption of the air out of the alveoli without replacing it
Global ventilation failure e.g airway obstruction, hypoventilation esp where tidal volume is very low- dead space is fixed, so as a proportion of each breath it gets higher as tidal volume reduces until there is minimal ALVEOLAR ventilation
How do we measure it?
Usually by infra-red absorption- CO2 absorbs infra-red light in a manner proportional to its concentration in the sampled gas.
Can be measured from a breathing circuit attached to an invasive airway device e.g supraglottic airway or endotracheal tube, or from a number of methods in the spontaneously breathing patient, such as a specific nasal cannula, or a sampling tube attached to an oxygen mask. Important to note that the waveform, and values for ETCO2 are very different in the spontaneously breathing patient, and we’ll come back to that later.
Might be measured directly from the breathing circuit (mainstream) or sucked out of the circuit in a sampling tube (sidestream).
Might display results as a waveform with a value given for ETCO2, or simply a number (capnometry) although the latter much less useful.
Colorimetric devices are available which change colour, based loosely on percentage of gas present. pH related. Occasionally used as an adjunct to waveform
What does the waveform mean?
The classic waveform that you will see in textbooks come from CO2 measured in the ventilated patient.
The graph has time in seconds along the x axis and partial pressure in kPa along the y axis
Phase I (inspiratory baseline) reflects inspired gas, which is normally devoid of carbon dioxide.
Phase II (expiratory upstroke) is the transition between dead space and alveolar gas from the respiratory bronchioles and alveoli.
Phase III is the alveolar plateau, when largely homogenous gas from the alveoli empties. This is the most accurate reflection of arterial co2
Phase 0 is the inspiratory downstroke, the beginning of the next inspiration
In the spontaneously breathing patient, there is not usually a plateau phase, which makes interpretation of ETCO2 values more difficult
All major anaesthetic organisations mandate the use of ETCO2 to confirm ETT placement
Good evidence that the trace is not completely flat even in cardiac arrest- Silvestri Ann Emerg Med 2005
Should seen >7 waveforms to exclude oesophageal (Orinato 1993)
Cardiac arrest- general
2010 & 2015 ERC guidelines recommend use of waveform capnography
Not new- 1978 paper Kalenda in Resuscitation described the use of capnogram as a guide to CPR efficacy
Grmec 2003 & 2011 in Critical Care
ETCO2 of >2.4kpa after 20min predictive of rosc , <1.3 = no ROSC
Alwens 2001 used cut off 10mmHg
Systematic review in 2013 Resuscitation used cut off of 1.3kPa but this wasn’t 100% sensitive across all studies
Concerns also raised by Norwegian paper in Resuscitation again 2011 showing a number of confounding factors made interpretation of etco2 problematic inc rhythm, bystander CPR, cause of arrest
As noted in 1978, ETCO2 drops off when chest compressions become ineffective.
Qvigstad et al showed in again in Resuscitation in 2013, confirming inter-individual variation in effectiveness of CPR using ETCO2 as a surrogate for CO
Deakin et al. (J. trauma 2004) showed that end-tidal CO2 may be of value in predicting outcome from major trauma (19). In a study of 191 blunt trauma patients, only 5% of patients with an end-tidal CO2 determination of 3.25 kPa survived to discharge
When should we use ETCO2 monitoring in the prehospital setting?
Mandatory if intubating (RSI, cardiac arrest)
Mandatory if performing procedural sedation where consciousness impaired
Highly recommended in cardiac arrest
Highly recommended in all critically ill patients
In cardiac arrest:
Attach to circuit/ BVM at soonest available opportunity
Use it to confirm intubation (if using)
Use it as a guide:
If ETCO2 has been steady during CPR but then begins to fall, consider changing rescuer
As corroborating evidence around decision making- if there has been no ROSC after 20min of full ALS protocol and ETCO2 remains below 1.3kPA, you are highly unlikely to resuscitate that patient
If there is a sudden increase in ETCO2- well done, you’ve achieved ROSC (even if you can’t yet feel a pulse- in fact, maybe you needn’t do a pulse check if you’ve got ETCO2)
Optimise ventilation post ROSC as you are now dealing with a head-injured patient.
In the critically ill patient:
If I can only have one monitor on an entrapped patient, I’d pick capnography
You will learn more quickly than any other method when your patient is deteriorating- e.g in blood loss, ETC02 will gradually fall. In the head injured patient who’s coning, you’ll see apnoeas and gradually rising ETCO2. In the heart failure patient who’s about to arrest, you’ll see their ETCO2 fall precipitously almost before anything else. In the comatose patient, you’ll be able to see that their airway is obstructed on the capnography a full 30 to 60s before their sats drop (by which point you’re already a long way down the oxygen dissociation curve).
You can also see when your treatment is working- if you give a patient in septic shock some fluid and improve their CO, you’ll see a rise in ETC02
You can confirm adequacy of respiratory function in the fitting or post-ictal patient when all other methods fail
Over-interpreting the accuracy of non-invasive capnography
Those lovely graphs showing curare clefts, rebreathing, bronchospasm etc you see on lots of different websites and in textbooks? They are almost all referring to capnography in the intubated and ventilated patient, who has a constant tidal volume.
Numbers are often wildly inaccurate in the critically unwell population, and there may be an ET-arterial gradient of 10kPA.
What CAN you tell from it? 1. Ventilation is occurring (accurate RR) 2. There is a cardiac output 3. You can interpret trends ie a gradual rise or fall in CO2, in the given clinical context 4. Very low is bad whichever way you look at it
Sometimes a low ETCO2 value is due to hyperventilation (because as we all remember, arterial CO2 concentration is almost linearly related to alveolar minute ventilation) BUT it may be hypoventilation with increased proportion of dead space ventilation compared to alveolar ventilation
Not using capnography
The more you use it, the more familiar with various patterns you will become
Stick it on everyone –it causes no harm. See what happens when you give a decent dose of morphine:
slows respiratory rate but breaths are normal volume
You get reduced alveolar MINUTE ventilation but normal alveolar TIDAL ventilation
Therefore what you see at ETCO2 is reasonably representative of arterial concentration because the same number of alveoli are ventilated and have opportunity to equilibrate with the blood CO2
This is unlike when a patient is making low tidal volume breaths, because then you’re largely ventilating dead space, and a much smaller number of alveoli are ventilated and thus equilibrium cannot occur between blood and gas
From: Capnography Outside the Operating Rooms, Anesthes. 2013;118(1):192-201. doi:10.1097/ALN.0b013e318278c8b6
A Prolonged phase II, increased α angle, and steeper phase III suggest bronchospasm or airway obstruction.
B Expiratory valve malfunction resulting in elevation of the baseline, and the angle between the alveolar plateau and the downstroke of inspiration is increased from 90°. This is due to rebreathing of expiratory gases from the expiratory limb during inspiration.
C Inspiratory valve malfunction resulting in rebreathing of expired gases from inspiratory limb during inspiration (reference 5 for details).
D Capnogram with normal phase II but with increased slope of phase III. This capnogram is observed in pregnant subjects under general anesthesia (normal physiologic variant and details in reference 9).
E Curare cleft: Patient is attempting to breathe during partial muscle paralysis. Surgical movements on the chest and abdomen can also result in the curare cleft.
F Baseline is elevated as a result of carbon dioxide rebreathing.
G Esophageal intubation resulting in the gastric washout of residual carbon dioxide and subsequent carbon dioxide will be zero.
H Spontaneously breathing carbon dioxide waveforms where phase III is not well delineated.
I Dual capnogram in one lung transplantation patient. The first peak in phase III is from the transplanted normal lung, whereas the second peak is from the native disease lung. A variation of dual capnogram (steeple sign capnogram – dotted line) is seen if there is a leak around the sidestream sensor port at the monitor. This is because of the dilution of expired PCO2with atmospheric air.
J Malignant hyperpyrexia where carbon dioxide is raising gradually with zero baseline suggesting increased carbon dioxide production with carbon dioxide absorption by the soda lime.
K Classic ripple effect during the expiratory pause showing cardiogenic oscillations. These occur as a result of to-and-for movement of expired gases at the sensor due to motion of the heartbeat during expiratory pause when respiratory frequency of mechanical ventilation is low. Ripple effect like wave forms also occur when forward flow of fresh gases from a source during expiratory pause intermingles with expiratory gases at the sensor.
L Sudden raise of baseline and the end-tidal PCO2(PETCO2) due to contamination of the sensor with secretions or water vapor. Gradual rise of baseline and PETCO2occurs when soda lime is exhausted.
M Intermittent mechanical ventilation (IMV) breaths in the midst of spontaneously breathing patient. A comparison of the height of spontaneous breaths compared to the mechanical breaths is useful to assess spontaneous ventilation during weaning process.
N Cardiopulmonary resuscitation: capnogram showing positive waveforms during each compression suggesting effective cardiac compression generating pulmonary blood.
O Capnogram showing rebreathing during inspiration. This is normal in rebreathing circuits such as Mapleson D or Bain circuit.
Difficult Airway Society 2015 guidelines for management of unanticipated difficult intubation in adults. C. Frerk et al. Difficult Airway Society: Intubation guidelines working group. British Journal of Anaesthesia, 115 (6): 827–848 (2015) doi:10.1093/bja/aev371
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Bennett, J. D., Guha, S. C., & Sankar, A. B. (1996). Cricothyrotomy: the anatomical basis. Journal of the Royal College of Surgeons of Edinburgh, 41(1), 57–60.
Boon, J. M., Abrahams, P. H., Meiring, J. H., & Welch, T. (2004). Cricothyroidotomy: a clinical anatomy review. Clinical Anatomy (New York, NY), 17(6), 478–486. http://doi.org/10.1002/ca.10231
Buonopane, C. E., Pasta, V., Sottile, D., Del Vecchio, L., Maturo, A., Merola, R., et al. (2014). Cricothyrotomy performed with the Melker™ set or the QuickTrach™ kit: procedure times, learning curves and operators’ preference. Il Giornale Di Chirurgia, 35(7-8), 165–170.
Cook, T., Woodall, N., & Frerk, C. (2015). Appendix 4 NAP4 Summary: major complications of airway management in the United Kingdom. British Journal of Anaesthesia (2011) 106 (5): 617-631. https://doi.org/10.1093/bja/aer058
Frerk, C., Mitchell, V. S., & McNarry, A. F. (2015). Difficult Airway Society 2015 guidelines for management of unanticipated difficult intubation in adults. British Journal of Anaesthesia (2015) 115 (6): 827-848. https://doi.org/10.1093/bja/aev371
Hubert, V., Duwat, A., Deransy, R., Mahjoub, Y., & Dupont, H. (2014). Effect of simulation training on compliance with difficult airway management algorithms, technical ability, and skills retention for emergency cricothyrotomy. Anesthesiology, 120(4), 999–1008. http://doi.org/10.1097/ALN.0000000000000138
Langvad, S., Hyldmo, P. K., Nakstad, A. R., Vist, G. E., & Sandberg, M. (2013a). Emergency cricothyrotomy–a systematic review. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine, 21, 43. http://doi.org/10.1186/1757-7241-21-43
Nakstad, A. R., Bredmose, P. P., & Sandberg, M. (2013). Comparison of a percutaneous device and the bougie-assisted surgical technique for emergency cricothyrotomy: an experimental study on a porcine model performed by air ambulance anaesthesiologists. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine, 21, 59. http://doi.org/10.1186/1757-7241-21-59
Prithishkumar, I. J., & David, S. S. (2010). Morphometric analysis and clinical application of the working dimensions of cricothyroid membrane in south Indian adults: With special relevance to surgical cricothyroidotomy. Emergency Medicine Australasia, 22(1), 13–20. http://doi.org/10.1111/j.1742-6723.2009.01245.x
The clinical anatomy of several invasive procedures. American Association of Clinical Anatomists, Educational Affairs Committee. (1999). The clinical anatomy of several invasive procedures. American Association of Clinical Anatomists, Educational Affairs Committee. Clinical Anatomy (New York, NY), 12(1), 43–54. http://doi.org/10.1002/(SICI)1098-2353(1999)12:1<43::AID-CA7>3.0.CO;2-W
Many apologies for the delay in the release of this podcast!
A second apology is due for the sound quality – it was recorded at a ‘live’ HEMS base – this has led to lots of background noise I am afraid. We have done our best to edit this out / reduce its effect but I’m afraid we are not experts in this area!
This podcast is part 2 of this series on the ventilator – and you should be familiar with the first in this series before progressing further!
Others have written excellent summaries of the themes of this podcast – please follow the links below:
This episode has been compiled over a year – many thanks to our four contributors, who have shared their stories and knowledge. They were interviewed at TraumaCare 2016, TraumaCare 2017 and the BASICS/FPHC Conference 2016.
If you ever need to talk about the impact of stresses and work experiences on you, please find a friend, colleague, GP, work Occupational Health Service, or one of the charities listed below.
Tony’s article describing his experience of providing medical care to those involved in the Shoreham air crash:
There is the potential for significant controversy in this month’s episode – and we would really appreciate the feedback of the prehospital community on this one.
We have held the ‘no clear fluids’ mantra close to our hearts for most of our prehospital careers. We ‘know’ that giving sea water to our patients, and diluting all of blood’s ‘good bits’ can’t be healthy. We believed in permissive hypotension – we were probably wrong.
Priorities for the bleeding trauma patient must include:
Minimum time to control of bleeding (tourniquets / haemostatics / knife / interventional radiology)
Appropriate choice of destination (knife / IR)
? Early correction of hypotension (especially if blunt trauma / associated head injury)
The balances of harms in the context of blunt trauma between the negative effects of infusing saline versus the negative effects of hypotension are unknown and prehospital actions need to be customised to an individual patient and situation.
In systems in which a potentially less harmful resuscitation strategy can be delivered sooner – PH systems with packed red cells / fresh frozen plasma / whole blood or freeze dried plasma, then it seems pragmatic to aim for normotension (predicted normal blood pressure) sooner in the patient’s care timeline than we have been e.g. at one hour. In patients with penetrating trauma permissive hypotension may remain useful for longer or at least until a patient can be differentiated and the bleeding controlled.
Penn-Barwell JG, Roberts SA, Midwinter MJ, Bishop JR: Improved survival in UK combat casualties from Iraq and Afghanistan: 2003-2012. J Trauma Acute Care Surg 78(5):1014–1020, 2015.
Holcomb JB, Donathan DP, Cotton BA, Del Junco DJ, Brown G, Wenckstern TV, Podbielski JM, Camp EA, Hobbs R, Bai Y, et al.: Prehospital transfusion of plasma and red blood cells in trauma patients. Prehosp Emerg Care 19(1):1–9, 2015.
Weaver AE, Eshelby S, Norton J, Lockey DJ: The introduction of on-scene blood transfusion in a civilian physician-led pre-hospital trauma service. Scand J Trauma Resusc Emerg Med 21(Suppl1):S27, 2013.
Bodnar D, Rashford S, Williams S, Enraght-Moony E, Parker L, Clarke B: The feasibility of civilian prehospital trauma teams carrying and administering packed red blood cells. Emerg Med J 31(2):93–95, 2014.
Thanks to Mark Forrest (@ObiDoc) for sharing these videos:
Spurr J, Gatward J, Joshi N, Carley SD. Top 10 (+1) tips to get started with in situ simulation in emergency and critical care departments. EMJ. 2016.
Bredmose PP, Habig K, Davies G, Grier G, Lockey D. Scenario based outdoor simulation in pre-hospital trauma care using a simple mannequin model. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine. 2010.
Patterson MD, Geis GL, Falcone RA, LeMaster T, Wears RL. In situ simulation: detection of safety threats and teamwork training in a high risk emergency department. BMJ Quality & Safety. 2013; 22: 468-477.
Boet S, Bould MD, Layat Burn C, Reeves S. Twelve tips for a successful interprofessional team-based high-fidelity simulation educational session. Medical Teacher. 2014; 36: 853-857.
Smith JE, Rikard A, Wise D. Traumatic Cardiac Arrest. Journal of the Royal Society of Medicine 2015. 108(1): 11-16.
Wise et al. Emergency thoracotomy: “how to do it”. EMJ; 2005: 22-24.
Hunt et al. Emergency thoracotomy in thoracic trauma: a review. Injury; 2006 (37): 1-19.
Clay et al. Emergency Department thoracotomy for the critically injured patient: Objectives, indications, and outcomes. World Journal of Emergency Surgery; 2006: 1:4.
Rhee et al. Survival after Emergency Department thoracotomy: review of published data for last 25 years. J Am Coll Surg; 2000. 190(3): 288-298
ACS Committee on Trauma Working Group. Practice Management guidelines for ED Thoracotomy. J Am Coll Surg. 2001, 193 (3): 303-309.
Editorial. When should we stop resuscitative efforts after blunt traumatic arrest. Injury; 2008 (39): 967-969.
Joint Position Statement of Nat Assoc EMS Physicians and ACS Committee on Trauma. Guidelines for withholding or termination of resuscitation in prehospital cardiopulmonary arrest. J Am Coll Surg; 2003 (1): 106-111.
Tarney et al.Outcomes following military traumatic cardiorespiratory arrest: A prospective observational study. Resuscitation; 2011: 1194-1197
The location of an injury and involvement of different structures defines the stability of a spinal injury.
Anterior column: anterior longitudinal ligament and the anterior half of the vertebral body/disc.
Middle column: posterior half of the vertebral body/disc and the posterior longitudinal ligament.
Posterior column: facet joints, ligamentum flavum, the spinous processes and the interconnecting ligaments.
An injury involving only the anterior column is considered to be stable, as will an isolated fracture of a spinous or transverse process. An unstable injury is one which involves all 3 columns and often one in which 2 columns are disrupted.
Stiell IG, Clement CM, McKnight RD, Brison R, Schull MJ, Rowe BH, et al. The Canadian C-spine rule versus the NEXUS low-risk criteria in patients with trauma. N Engl J Med. 2003 Dec 25;349(26):2510–8.
Oteir AO, Smith K, Stoelwinder JU, Middleton J, Jennings PA. Should suspected cervical spinal cord injury be immobilised?: A systematic review. Injury. Elsevier Ltd; 2015 Apr 1;46(4):528–35.
Smyth M, Cooke MW. Value of a rigid collar: in need of more research and better devices. Emergency Medicine Journal. 2013 May 13;30(6):516–6.
Crane T, Cooke MW, Wellings R, Wayte S, Higgins J. MRI study of effectiveness of cervical spine immobilisation- a pilot study. The University of Warwick. 2007 Aug 1;:1–18.
BOAST2: SPINAL CLEARANCE IN THE TRAUMA PATIENT. British Orthopaedic Association Standards for Trauma (BOAST); 2008. 1 p.
Hauswald M, Ong G, Tandberg D, Omar Z. Out-of-hospital spinal immobilization: its effect on neurologic injury. Acad Emerg Med. 2008 Apr 15;5(3):214–9.
Prasarn ML, Horodyski M, Dubose D, Small J, Del Rossi G, Zhou H, et al. Total Motion Generated in the Unstable Cervical Spine During Management of the Typical Trauma Patient. Spine. 2012 May;37(11):937–42.
Gill DS, Mitra B, Reeves F, Cameron PA, Fitzgerald M, Liew S, et al. Can initial clinical assessment exclude thoracolumbar vertebral injury? Emergency Medicine Journal. 2013 Jul 19;30(8):679–82.
Leech C, Porter K, Bosanko C. Log-rolling a blunt major trauma patient is inappropriate in the primary survey. Emergency Medicine Journal. 2013 Dec 22;31(1):86–6.
Horodyski M, Conrad BP, Del Rossi G, DiPaola CP, Rechtine GR II. Removing a Patient From the Spine Board: Is the Lift and Slide Safer Than the Log Roll? J Trauma. 2011 May;70(5):1282–5.
I J, A M, Yu E, Tulman D, Jones C, Stawicki S. A systematic review of the need for MRI for the clearance of cervical spine injury in obtunded blunt trauma patients afternormal cervical spine CT. Journal of Emergencies, Trauma, and Shock. 2014 Feb 11;7(4):251–5.
Sundstrøm T, Asbjørnsen H, Habiba S, Sunde GA, Wester K. Prehospital Use of Cervical Collars in Trauma Patients: A Critical Review. J Neurotrauma. 2014 Mar 15;31(6):531–40.
Armstrong BP, Simpson HK, Crouch R, Deakin CD. Prehospital clearance of the cervical spine: does it need to be a pain in the neck? Emerg Med J. 2007 Jul 1;24(7):501–3.
Connor D, Greaves I, Porter K, Bloch M, consensus group Faculty of Pre-Hospital Care. Pre-hospital spinal immobilisation: an initial consensus statement. Emerg Med J. 2013 Dec 1;30(12):1067–9.
Fattah S, Johnsen AS, Andersen JE, Vigerust T, Olsen T, Rehn M. Rapid extrication of entrapped victims in motor vehicle wreckage using a Norwegian chainmethod – cross-sectional and feasibility study. 2014 Jul 3;14(1):1–5.
Stiell IG, Nesbitt LP, Pickett W, Munkley D, Spaite DW, Banek J, et al. The OPALS Major Trauma Study: impact of advanced life-support on survival and morbidity. CMAJ. 2008 Apr 22;178(9):1141–52.
Edwards MA, Verwey J, Herbert S, Horne S, Smith JE. Cervical spine clearance in the elderly: do elderly patients get a bad deal? Emerg Med J. 2013 May 23.
Sundstrøm T, Asbjørnsen H, Habiba S, Sunde GA, Wester K. Prehospital Use of Cervical Collars in Trauma Patients: A Critical Review. J Neurotrauma. 2014 Mar 15;31(6):531–40.
Shafer JS, Naunheim RS. Cervical spine motion during extrication: a pilot study. West J Emerg Med. 2009 May;10(2):74–8.
Davis JW, Phreaner DL, Hoyt DB, Mackersie RC. The etiology of missed cervical spine injuries. J Trauma. 1993 Mar;34(3):342–6.
Hale DF, Fitzpatrick CM, Doski JJ, Stewart RM, Mueller DL. Absence of clinical findings reliably excludes unstable cervical spine injuries in children 5 years or younger. Journal of Trauma and Acute Care Surgery. 2015 May;78(5):943–8.
Benger J, Blackham J. Why do we put cervical collars on conscious trauma patients? Scand J Trauma Resusc Emerg Med. 2009;17(1):44.
We have talked about ramping previously, in Episode 6: Oxygenation. This is how a pregnant patient should be positioned for airway manoeuvres and interventions, for example induction of anaesthesia and intubation.
The ILCOR 2015 update pertaining to Cardiac Arrest Associated with Pregnancy is accessible here:
Clark SL, Cotton DB, Pivarnik JM et al. Position change and central hemodynamic profile during normal third trimester pregnancy and post partum. Am J Obstetrics & Gynaecology. 1991; 164: 883-887.
Bamber JH, Dresner M. Aortocaval compression in pregnancy: the effect of changing the degree and direction of lateral tilt on maternal cardiac output. Anaesthesia & Analgesia. 2003; 97: 256-258.
Lee SWY, Khaw KS, Kee WN, Leung TY, Critchley LAH. Haemodynamic effects from aortocaval compression at different angles of lateral tilt in non-labouring term pregnant women. British Journal of Anaesthesia. 2012; 109: 950-956.
We hope you enjoyed our sepsis podcast. It is obviously a huge topic and there is lots of information to cover; a couple of other recently released podcasts are available which are produced with the Emergency Medicine community in mind, but will no doubt expand your knowledge.
It was a single centre study which compared standard care with protocolised resuscitation packaged together as early goal-directed therapy (EGDT). This is what the study did:
As you will see the trial was relatively small – with only 263 patients being recruited into the trial. What was impressive, and changed practice, forming the basis of the Surviving Sepsis Campaign, was the significant reduction in mortality. Patients in the standard care group had a mortality of 46% compared with the treatment group 30%, which was statistically significant (p=0.009).
Further large randomized controlled studies to try and demonstrate the same mortality benefit from Rivers-style EGDT have not shown the same results (Process, Arise, PROMISe). Patients in these trials were randomly assigned to one of two groups. The ‘intervention’ group received the new treatment, in this case EGDT, which was being tested. The ‘standard care’ group were looked after according to how the clinician would usually treat a patient with severe sepsis. This was the same principle as in the Rivers trial: the standard care group is the ‘control’ group against which changes in outcome for the ‘intervention’ group are compared. The mortality in both groups in all 3 trials was similar, there was not the significant reduction in mortality seen in the Rivers study. This was probably because, as we say in the podcast, ‘standard’ care for sepsis has improved considerably in the intervening years. The control group received many similar treatments as the ‘intervention’ group (just not full protocolised EGDT) highlighting that with good sepsis care (fluid resuscitation, close monitoring, early appropriate antibiotic administration), mortality can be reduced.
Red flag sepsis is a way of identifying those patients with sepsis who are high risk and who warrant immediate treatment:
Have a look at the UK Sepsis Trust website: http://sepsistrust.org. There are toolkits available to download, including one specifically written for the prehospital environment with the College of Paramedics, which summarises the recognition and management of sepsis.
Reviewed (again for the Emergency Medicine community) here.
When Tim talks about test characteristics he is referring to the ability of a test to correctly identify the presence or absence of an illness. Some may think that if a test is positive it always means the patient has the illness, or indeed if it is negative it rules out the possibility of that illness but this is not the case with many of the tests we use.
Think about ECG as an example, So, where the box is green, the test has given us the correct result for the patient. But, where the box is red the test has given us the incorrect result: you will all be able to think about patients in whom the ECG was normal, but the patient turned out to have had an MI, or when the ECG showed an MI but the patient turned out not to have had one. These tables are used when assessing the usefulness of a test (or it’s sensitivity and specificity), and, when researching how useful tests are we need the majority of patients to fall into the green boxes.
We will put together a podcast on test characteristics over the next couple of months, which will explain this in more detail. An amazing podcast on the subject can be found at SMART EM: SMART Testing: Back to Basics
As always, any feedback, comments etc. – please let us know on the blog below!
Herlitz J, ng AB, m BW-S, Axelsson C, Bremer A, Hagiwara M, et al. Suspicion and treatment of severe sepsis. An overview of the prehospital chain of care. Scand J Trauma Resusc Emerg Med. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine; 2012 Jun 27;20(1):1–1.
Studnek JR, Artho MR, Garner CL, Jones AE. The impact of emergency medical services on the ED care of severe sepsis. Am J Emerg Med. 2012 Jan;30(1):51–6.
Puskarich MA, Marchick MR, Kline JA, Steuerwald MT, Jones AE. One year mortality of patients treated with an emergency department based early goal directed therapy protocol for severe sepsis and septic shock: a before and after study. Crit Care. 2009;13(5):R167.
Seymour CW, Rea TD, Kahn JM, Walkey AJ, Yealy DM, Angus DC. Severe Sepsis in Pre-Hospital Emergency Care. Am J Respir Crit Care Med. 2012 Dec 15;186(12):1264–71.
Band RA, Gaieski DF, Hylton JH, Shofer FS, Goyal M, Meisel ZF. Arriving by Emergency Medical Services Improves Time to Treatment Endpoints for Patients With Severe Sepsis or Septic Shock. Academic Emergency Medicine. 2011 Aug 30;18(9):934–40.
Seymour CW, Cooke CR, Heckbert SR, Spertus JA, Callaway CW, Martin-Gill C, et al. Prehospital intravenous access and fluid resuscitation in severe sepsis: an observational cohort study. 2014 Oct 28;:1–9.
Trust US. You Gov Poll – Public Awareness of Sepsis. UK Sepsis Trust; 2014 Nov pp. 1–1.
MD GEH, MD RET, MD RS, MD JDL, BS AMB, BS AJS, et al. ACCEPTED MANUSCRIPT. Am J Emerg Med. Elsevier B.V; 2015 Aug 26;:1–31.
Amado Alejandro Baez MD MSc MFFF, MD LC. ACCEPTED MANUSCRIPT. Am J Emerg Med. Elsevier B.V; 2015 Oct 17;:1–16.
Guerra WF, Mayfield TR, Meyers MS, Clouatre AE, Riccio JC. Early detection and treatment of patients with severe sepsis by prehospital personnel. J Emerg Med. 2013 Jun;44(6):1116–25.
Gaieski DF, Mikkelsen ME, Band RA, Pines JM, Massone R, Furia FF, et al. Impact of time to antibiotics on survival in patients with severe sepsis or septic shock in whom early goal-directed therapy was initiated in the emergency department*. Crit Care Med. 2010 Apr;38(4):1045–53.
Yealy DM, Huang DT, Delaney A, Knight M, Randolph AG, Daniels R, et al. Recognizing and managing sepsis: what needs to be done? ??? ??? 2015 Apr 24;:1–10.
Báez AA, Hanudel P, Perez MT, Giráldez EM, Wilcox SR. Prehospital Sepsis Project (PSP): knowledge and attitudes of United States advanced out-of-hospital care providers. Prehosp Disaster Med. 2013 Apr;28(2):104–6.
Harnden A. Parenteral penicillin for children with meningococcal disease before hospital admission: case-control study. BMJ. 2006 Jun 3;332(7553):1295–8.
Femling J, Weiss S, Hauswald E. EMS Patients and Walk-In Patients Presenting With Severe Sepsis: Differences in Management and Outcome. South Med J. 2014.
Gray A, Ward K, Lees F, Dewar C, Dickie S, McGuffie C, et al. The epidemiology of adults with severe sepsis and septic shock in Scottish emergency departments. Emergency Medicine Journal. 2013 Apr 12;30(5):397–401.
Seymour CW, Cooke CR, Mikkelsen ME, Hylton J, Rea TD, Goss CH, et al. Out-of-hospital fluid in severe sepsis: effect on early resuscitation in the emergency department. Prehosp Emerg Care. 2010 Apr;14(2):145–52.
Hahné SJM, Charlett A, Purcell B, Samuelsson S, Camaroni I, Ehrhard I, et al. Effectiveness of antibiotics given before admission in reducing mortality from meningococcal disease: systematic review. BMJ. 2006 Jun 3;332(7553):1299–303.
Wang HE, Weaver MD, Shapiro NI, Yealy DM. Opportunities for Emergency Medical Services care of sepsis. Resuscitation. 2010 Feb;81(2):193–7
To provide a bit of balance following our earlier hyperoxia podcast, this episode we are discussing circumstances when we want to deliver extra oxygen to patients and ways to do this effectively, including an interview with Sydney HEMS Consultant Yash Wilmalasena on apnoeic oxygenation. Hope you find it useful!
Some of the stuff we talked about:
Optimal patient positioning when managing the airway and assisting ventilation has traditionally been taught as ‘sniffing the morning air’, shown here.
But now, learning from bariatric practice we are realising that ramping is better for airway optimisation. In this position the patient’s tragus is lined up with their sternal notch to make the airway as straight as possible.
This is a great (and entertaining!) video cast from Emergency Medicine colleagues in the States discussing and demonstrating techniques for optimal bag-valve-mask ventilation.
Wilmalasena Y, Burns B, Reid C, Ware S., Habig K. Apneic oxygenation was associated with decreased desaturation rates during rapid sequence intubation by an Australian helicopter emergency medicine service. Annals of Emergency Medicine. 2015; 65(4): 371-376.
Weingart SD, Levitan RM. Preoxygenation and Prevention of Desaturation During Emergency Airway Management. Annals of Emergency Medicine. 2012; 59(3): 165-175.
Weingart SD, Trueger NS, Wong N, Scofi J, Singh N, Rudolph SS. Delayed Sequence Intubation: A Prospective Observational Study. Annals of Emergency Medicine. 2014; 65(4): 349-355.
Weingart SD. Preoxygenation, reoxygenation, and delayed sequence intubation in the Emergency Department. The Journal of Emergency Medicine. 2010;
Grant S, Khan F, Keijzers G, Shirran M, Marneros L. Ventilator-assisted preoxygenation: protocol for combining non-invasive ventilation and apnoeic oxygenation using a portable ventilator. Emergency Medicine Australasia. 2016: 28(1); 67-72.
Von Goedecke A, Wenzel V, Hormann C, Voelckel WG, Wagner-Berger HG, Zecha-Stallinger A, Luger TJ, Keller C. Effects of face mask ventilation in apneic patients with a resuscitation ventilator in comparision with a bag-valve-mask. Journal of Emergency Medicine. 2006: 30(1); 63-67.
Semier MW, Janz DR, Lentz RJ, Matthews DT, Norman BC, Assad TR, Keriwala RD, Ferrell BA, Noto MJ, McKown AC, Kocurek EG, Warren MA, Huerta LE, Rice TW. Randomized trial of apneic oxygenation during endotracheal intubation of the critically ill. American Journal of Respiratory Critical Care Medicine. 2016; 193(3): 273-280. (FELLOW Trial)
Chilcott RP. Managing mass casualties and decontamination. Environmental International. 2014; 72: 37-45.
This is the Step 1,2,3 tool described:
For more information on the toxidromes associated with various chemicals, biological agents and radiation sources have a look at this document (admittedly it’s a few years old but the content is still good, especially the flow chart which is pasted below):
Anti-muscarinic = blocking the muscarinic receptors, ie blocking the effect of acetylcholine, hence also called anti-cholinergic. Impacts on parasympathetic stimulation. Antimuscarinic effects include dilated pupils (leading to blurred vision), reduced secretion of saliva (hence dry mouth), sweat and digestive juices. Relaxation of smooth muscle causing urinary retention, ileus. Also tachycardia, confusion progressing to delirum/coma.
Nerve agents inhibit anticholinesterase therefore there is an excess of acetylcholine resulting in opposite features: diarrhoea, urination, miosis, increased bronchial secretions, bronchoconstriction, vomiting, lacrimation, salivation.
Always ahead of the curve… St Emlyns have recently published a blog post on this very topic! It’s great, so have a read:
Hello and welcome to our next episode – we hope you enjoy it. This episode concentrates on hyperoxia – the delivery of lots (often too much) oxygen and the harms it may cause our patients. We both had colds – many apologies for the blocked noses and many sniffs!
We hope you find it useful.
To follow: Dr Matt Thomas from the Great Western Air Ambulance discussing his groups work around reducing hyperoxia post-rosc.
Cornet AD, Kooter AJ, Peters MJL, Smulders YM. The potential harm of oxygen therapy in medical emergencies. Crit Care. 2013 Apr 11;17(2):313.
Rincon F, Kang J, Maltenfort M, Vibbert M, Urtecho J, Athar MK, et al. Association Between Hyperoxia and Mortality After Stroke. Crit Care Med. 2014 Feb;42(2):387–96.
Stub D, Smith K, Bernard S, Bray J, Stephenson M, Cameron P, et al. A randomized controlled trial of oxygen therapy inacute myocardial infarction Air Verses Oxygen InmyocarDial infarction study (AVOID Study). American Heart Journal. Mosby, Inc; 2012 Mar 1;163(3):339–345.e1. 3. Asfar P, Singer M, Radermacher P. Understanding the benefits and harms of oxygen therapy. Intensive Care Med. 2015 Jan 30.
Calzia E, Asfar P, Hauser B, Matejovic M, Ballestra C, Radermacher P, et al. Hyperoxia may be beneficial. Crit Care Med. 2010 Oct;38:S559–68.
Asfar P, Calzia E, Huber-Lang M, Ignatius A, Radermacher P. Hyperoxia during septic shock–Dr. Jekyll or Mr. Hyde? Shock. 2011 Nov 21;37(1):122–3.
Cornet AD, Kooter AJ, Peters MJL, Smulders YM. The potential harm of oxygen therapy in medical emergencies. Crit Care. 2013 Apr 11;17(2):313.
Ligtenberg JJM, Stolmeijer R, Broekema JJ, Maaten ter JC, Zijlstra JG. A little less saturation? Crit Care. 2013 Jun 12;17(3):439.
Sorry for the slight delay releasing our “October” podcast – but here it is (note how it is cunningly labelled Episode 2)! This month we are reviewing the evidence for the pelvic binder and discussing scenarios in which it should (and should not) be used.
As always, please get in touch with questions and comments, either via the blog, twitter or email email@example.com
This is where the greater trochanters are:
This is where a binder should sit on the pelvis – it commonly ends up higher, either in application or ‘rides up’ during transfer – keep an eye on it!
These are the different types of fracture pattern that can occur in a pelvic fracture: of course patients can suffer from multiple force vectors so may end up with any combination of these fracture types.
Please click on this link below for our video on using a scoop to insert the pelvic binder…
As always… Get in touch!
Scott I, Porter K, Laird C, Greaves I, Bloch M. The prehospital management of pelvic fractures: initial consensus statement. EMJ. 2013; 30(12): 1070-1072.
Lee C, Porter K. The prehospital management of pelvic fractures. EMJ. 2007; 24: 130-133.
Prasarn ML, Conrad B, Small J, Horodyski M, Rechtine GR. Comparison of circumferential pelvic sheeting versus the T-POD on unstable pelvic injuries: A cadaveric study of stability. Injury. 2013; 44: 1756-1759.
Trebilcock H. Reducing overtriage and undertriage rates if pelvic fractures and unnecessary pelvic binder applications in major trauma patients. EMJ. 2015; 32(6): e17.
DeAngelis NA, Wixted JJ, Drew J, Eskander MS, Eskander JP, French BG. Use of the trauma pelvic orthotic device (T-POD) for provisional stabilisation of anterior-posterior compression type pelvic fractures: A cadaveric study. Injury. 2008; 39: 903-906.
Bottlang M, Krieg JC, Mohr M, Simpson TS, Madey SM. Emergent management of pelvic ring fractures with use of circumferential compression. The Journal of Bone & Joint Surgery. 2002; 84A (2): 43-47.
Tan ECTH, van Stigt SFL, van Vugt AB. Effect of a new pelvic stabilizer (T-POD) on reduction of pelvic volume and haemodynamic stability in unstable pelvic fractures. Injury. 2010; 41(12): 1239-1243.
Knops SP, Van Lieshout EMM, Spanjersberg WR, Patka P, Schipper IB. Randomised clinical trial comparing pressure characteristics of pelvic circumferential compression devices in healthy volunteers. Injury. 2011; 42(10): 1020-1026.
Mason LW, Boyce DE, Pallister I. Catastrophic myonecrosis following circumferential pelvic binding after massive crush injury: A case report. Injury Extra. 2009: 84-86.
Stewart M. BestBet: Pelvic circumferential compression devices for haemorrhage control: panacea or myth. EMJ. 2013; 30: 425-426.
Croce MA, Magnotti LJ, Savage SA, Wood GW, Fabian TC. Emergent pelvic fixation in patients with exsanguinating pelvic fractures. Journal of American College of Surgeons. 2007; 204: 935-942.
Knops SP, Schep NWL, Spoor CW, van Riel MPJM, Spanjersberg WR, Kleinrensink GJ, van Lieshout EMM, Patka P, Schipper IB. Comparison of three different pelvic circumferential compression devices: A biomechanical cadaver study. Journal of Bone & Joint Surgery. 2011; 93: 230-240.
Knops SP, van Riel MPJM, Goossens RHM, Lieshout EMM, Patka P, Schipper IB. Measurements of the exerted pressure by pelvic circumferential compression devices. The Open Orthopaedics Journal. 2010; 4: 101-106.
Here it is – our very first podcast, and guess what – it is on supraglottic airways!
This first episode reviews the history of the laryngeal mask airway and we discuss the relative benefits and risks of supraglottic airway devices. We’ve interviewed Dr Rob Moss, author of the Faculty of Prehospital Care (FPHC) Consensus Guidelines on pharmacologically assisted laryngeal mask (PALM) insertion. Click here for the link to the guideline.
We also met Professor Jonathan Benger and discuss the role of supraglottic devices in patients in cardiac arrest. Please have a look at the airways 2 trial website here.
References and resources:
Benger JR, Voss S, Coates D, Greenwood R, Nolan J, Rawstorne S, et al. Randomised comparison of the effectiveness of the laryngeal mask airway supreme, i-gel and current practice in the initial airway management of prehospital cardiac arrest (REVIVE-Airways): a feasibility study research protocol. BMJ Open. 2013 Jan 31;3(2):e002467–7.
Berlac P, Hyldmo PK, Kongstad P, Kurola J, Nakstad AR, Sandberg M. Pre-hospital airway management: guidelines from a task force from the Scandinavian Society for Anaesthesiology and Intensive Care Medicine. Acta Anaesthesiol Scand. 2008 Jul 9;52(7):897–907.
Bosch J, de Nooij J, de Visser M, Cannegieter SC, Terpstra NJ, Heringhaus C, et al. Prehospital use in emergency patients of a laryngeal mask airway by ambulance paramedics is a safe and effective alternative for endotracheal intubation. Emergency Medicine Journal. 2014 Aug 14;31(9):750–3.
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Deakin CD, Clarke T, Nolan J, Zideman DA, Gwinnutt C, Moore F, et al. A critical reassessment of ambulance service airway management in prehospital care: Joint Royal Colleges Ambulance Liaison Committee Airway Working Group, June 2008. Emergency Medicine Journal. 2010 Mar 19;27(3):226–33.
Deakin CD, Peters R, Tomlinson P, Cassidy M. Securing the prehospital airway: a comparison of laryngeal mask insertion and endotracheal intubation by UK paramedics. Emergency Medicine Journal. 2004 Dec 20;22(1):64–7.
Gruber C, Nabecker S, Wohlfarth P, Ruetzler A, Roth D, Kimberger O, et al. Evaluation of airway management associated hands-off time during cardiopulmonary resuscitation: a randomised manikin follow-up study. Scand J Trauma Resusc Emerg Med. 2013;21:10.
Hasegawa K, Hiraide A, Chang Y, Brown DFM. Association of prehospital advanced airway management with neurologic outcome and survival in patients with out-of-hospital cardiac arrest. JAMA. 2013 Jan 16;309(3):257–66.
Kajino K, Iwami T, Kitamura T, Daya M, Ong ME. Comparison of supraglottic airway versus endotracheal intubation for the pre-hospital treatment of out-of-hospital cardiac arrest. Crit Care. 2011.
Mason AM. Prehospital Use of the Intubating Laryngeal Mask Airway in Patients with Severe Polytrauma: A Case Series. Case Reports in Medicine. 2009;2009(3):1–7.
Middleton PM, Simpson PM, Thomas RE, Bendall JC. Higher insertion success with the i-gel® supraglottic airway in out-of-hospital cardiac arrest: A randomised controlled trial. Resuscitation. 2014 Jul;85(7):893–7.
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Ostermayer DG, Gausche-Hill M. Supraglottic Airways: The History and Current State of Prehospital Airway Adjuncts. Prehosp Emerg Care. 2014 Jan;18(1):106–15.